Abstract
Platelets are produced from megakaryocytes. Under normal physiological conditions changes in platelet volume and density are not secondary to ageing but are present at thrombopoiesis. Prolonged increased platelet destruction rate leads to the production of large platelets from large, high ploidy megakaryocytes. In vivo and ex vivo studies show such platelets have more haemostatic potential. Platelets are larger and denser in acute myocardial infarction, where bleeding time is shortened and bleeding time aspirin sensitivity is increased. Thromboxane A(2) formation is increased in unstable angina pectoris and in acute myocardial infarction. Megakaryocytes are enlarged in acute myocardial infarction and in sudden unexpected cardiac death. Megakaryocyte and platelet changes may precede coronary artery thrombosis.
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